Jasmer and colleagues (1) may be overestimating the role of molecular epidemiologic analysis in tuberculosis control. The tuberculosis control measures that were reportedly intensified appear to represent well-known traditional principles and arguably should have been in place already. Could it not be argued that the only variable truly affecting clustering of tuberculosis cases was the decline in HIV-tuberculosis co-infection? The local rate of HIV-infected patients with tuberculosis decreased to 16% in 1996 and 5% in 1997. What percentage of clustered cases involved HIV-infected persons? Although DNA fingerprinting enables us to assign individual cases of tuberculosis to clusters, it is probably not true that this knowledge will allow tuberculosis control programs to directly affect the clustering phenomenon. Clustering occurs either because the case contact is immunocompromised and progresses rapidly to disease after exposure or because the index case-patient has chronic, far-advanced disease before seeking medical attention. In the latter situation, so many months elapse that secondary cases of tuberculosis develop. A tuberculosis control program cannot directly influence either situation.